Baby bottles are often made of polycarbonate plastic. Impurities remaining in the bottle from the monomer bisphenol A can migrate from the plastic bottles into baby food, thereby causing a health concern. Previous migration testing of new baby bottles showed only trace migration levels of the substance. In the present work, polycarbonate baby bottles were subjected to simulated use by dishwashing, boiling and brushing. Migration testing performed with both new and used bottles revealed a significant increase in migration of bisphenol A due to use. This finding might be explained by polymer degradation. Bisphenol A was determined in 200-ml samples of water food simulant by a method based on solid-phase extraction followed by gas chromatography coupled with mass spectrometry. The detection limit was 0.1 µg l⁻¹. Twelve different polycarbonate baby bottles were tested by filling them with hot water (100°C) for 1 h. The mean bisphenol A level from new bottles was 0.23 + − 0.12 µg l⁻¹, while the mean levels from bottles subjected to simulated use were 8.4 + − 4 µg l⁻¹ (dishwashed 51 times) and 6.7 + − 4 µg l⁻¹ (dishwashed 169 times), respectively. None of the bottles released bisphenol A at levels that exceed the recently established provisional tolerable daily intake (0.01 mg kg⁻¹ body weight/day) in the European Union.

The flavonoid pathway is known to be up‐regulated by different environmental stress factors. Down‐regulation of the pathway is much less studied and is emphasized in the present work. Flavonoid accumulation was induced by exposing plants for 1 week to nitrogen depletion at 10 °C, giving high levels of anthocyanins and 3‐glucoside‐7‐rhamnosides, 3,7‐di‐rhamnosides and 3‐rutinoside‐7‐rhamnosides of kaempferol and quercetin. Flavonol accumulation as influenced by temperatures and nitrogen supply was not related to the glycosylation patterns but to the classification as quercetin and kaempferol. When nitrogen was re‐supplied, transcripts for main regulators of the pathway, PAP1/GL3 and PAP2/MYB12, fell to less than 1 and 0.1% of initial values, respectively, during 24 h in the 15–30 °C temperature range. Anthocyanins showed a half‐life of approximately 1 d, while the degradation of flavonols was much slower. Interestingly, the initial fluxes of anthocyanin and flavonol degradations were found to be temperature‐independent. A kinetic model for the flavonoid pathway was constructed. In order to get the observed concentration‐temperature profiles as well as the temperature compensation in the flavonoid degradation flux, the model predicts that the flavonoid pathway shows an increased temperature sensitivity at the end of the pathway, where the up‐regulation by PAP/GL3 has been found to be largest.

The progressive loss of motor control due to reduction of dopamine-producing neurons in the substantia nigra pars compacta and decreased striatal dopamine levels are the classically described features of Parkinson disease (PD). Neuronal damage also progresses to other regions of the brain, and additional non-motor dysfunctions are common. Accumulation of environmental toxins, such as pesticides and metals, are suggested risk factors for the development of typical late onset PD, although genetic factors seem to be substantial in early onset cases. Mutations of DJ-1 are known to cause a form of recessive early onset Parkinson disease, highlighting an important functional role for DJ-1 in early disease prevention. This study identifies human DJ-1 as a metal-binding protein able to evidently bind copper as well as toxic mercury ions in vitro. The study further characterizes the cytoprotective function of DJ-1 and PD-mutated variants of DJ-1 with respect to induced metal cytotoxicity. The results show that expression of DJ-1 enhances the cells' protective mechanisms against induced metal toxicity and that this protection is lost for DJ-1 PD mutations A104T and D149A. The study also shows that oxidation site-mutated DJ-1 C106A retains its ability to protect cells. We also show that concomitant addition of dopamine exposure sensitizes cells to metal-induced cytotoxicity. We also confirm that redox-active dopamine adducts enhance metal-catalyzed oxidation of intracellular proteins in vivo by use of live cell imaging of redox-sensitive S3roGFP. The study indicates that even a small genetic alteration can sensitize cells to metal-induced cell death, a finding that may revive the interest in exogenous factors in the etiology of PD.

A procedure used by the Norwegian Food Safety Authority for surveillance of contaminants from plastic food contact materials (polyolefin drinking bottles, water boilers, polyamide cooking utensils and plastic multi-layer materials) is described. It is based on gas chromatographic-mass spectrometric (GC/MS) analysis of food simulants exposed to plastic materials. Most migrants were substances not-intentionally added to the plastic (degradation products, impurities) or originated from non-plastic components, such as printing inks, adhesives, not-listed additives, solvents and coatings. Hence, the majority of the identified migrants were regulated by the general statements in the EU Framework Regulation, which neither specify limits nor requirements regarding risk assessment, rather than by specific migration controls. Risk assessment has been carried out for selected non-authorized substances. The analysis and the management of these substances and materials with respect to safety represents a challenge to the food authorities.